SMN1 KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control provided.
BCD541, Component of gems 1, Gemin-1, OTTHUMP00000125198, OTTHUMP00000223567, OTTHUMP00000223568, OTTHUMP00000224066, OTTHUMP00000226924, SMA, SMA 1, SMA 2, SMA 3, SMA 4, SMN1, SMN2, SMNT, SMN_HUMAN, Survival motor neuron protein, Survival of motor neuron 1, telomeric, T-BCD541
SMN1 KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control provided.
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.
Recommended control: Human wild-type HCT116 cell line (ab273730). Please note a wild-type cell line is not automatically included with a knockout cell line order, if required please add recommended wild-type cell line at no additional cost using the code WILDTYPE-TMTK1.
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our limited use license and patent pages.
SMN also known as Survival of Motor Neuron protein or Gemin 1 is an important protein involved in the assembly of small nuclear ribonucleoproteins (snRNPs). It has a molecular mass of approximately 38 kDa. SMN proteins are expressed in almost all tissues with highest levels in spinal cord and brain tissues. They play a mechanical role in Gemin complex assisting RNA processing tasks which are essential in RNA metabolism alongside other Gemin proteins.
The SMN protein operates within the SMN-Gemin complex a multi-protein assembly important for snRNP biogenesis and pre-mRNA splicing. This complex coordinates the maturation and transport of snRNPs facilitating the processing of precursor mRNAs in the nucleus. SMN and associated Gemin proteins mediate the assembly of Sm proteins onto snRNA ensuring accurate splicing mechanisms necessary for gene expression.
The SMN protein is notably involved in the chaperone-assisted assembly pathway related to snRNP biogenesis. It plays a central role in the spliceosome assembly process working closely with Sm proteins and other RNA-binding proteins. Importantly SMN interacts with the ribonucleoprotein complex influencing mRNA splicing which integrates into the broader cell signaling pathways such as the cholinergic agonist pathways and RNA splicing pathways that regulate neuromuscular communication.
The deficiency or malfunction of SMN protein directly relates to Spinal Muscular Atrophy (SMA) an autosomal recessive disorder. SMA is characterized by motor neuron degeneration which can be attributed to insufficient SMN protein levels leading to compromised snRNP assembly and splicing. The SMN1 gene deletion or mutation reduces the available SMN protein linking this defect with the severity of SMA. Studies suggest that altering the expression levels of the related SMN2 gene can potentially modulate disease outcomes further emphasizing the connection between SMN protein and SMA pathogenesis.
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6 bp deletion after Thr289 (allele 1) and 11 bp deletion after Trp286 (allele 2) of the WT protein
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